TECHNOLOGY TO WATCH FINALLY, HOPE FOR CURING ALZHEIMER'S Scientists are starting to learn how the debilitating disease attacks critical mechanisms of the brain -- at least in hereditary cases.

(FORTUNE Magazine) – Researchers may at last have found a promising path toward treatment of Alzheimer's disease. No one has yet discovered a way to stop or slow down this devastating malfunction of the brain, which robs its victims of memory, judgment, and emotional stability. Alzheimer's is invariably accompanied by lesions called senile plaques. But do the plaques cause the disease, or are they a result of it? Evidence is rapidly piling up that the plaques can indeed set off Alzheimer's, and these discoveries have opened a brand-new avenue for treating the disease with novel drugs. The plaques seem to poison nearby neurons, causing the nerve cells to degenerate. The heaviest accumulation of plaques takes place in the areas of the brain most responsible for cognition and memory, notably the cerebral cortex and the hippocampus (see diagram). Hence Alzheimer's cruel legacy: Its sufferers can move around unassisted, since the disease has little effect on the motor functions controlled by other parts of the brain, but the victims forget where they are or where they are going. Most big drug manufacturers have been working on synthetic facsimiles of neurotransmitters, chemicals that normally carry signals between neurons but become depleted in Alzheimer's. Those chemicals, however, won't bring dying or dead neurons back to life. None of these conventional ''Band-Aid'' drugs has been approved by the Food and Drug Administration. As the cause of Alzheimer's finally becomes clearer, a better way to deal with the damage may be in sight. New research shows that a substance called beta amyloid precursor protein (beta-APP) is responsible for plaque formation. Its normal function isn't fully understood, but whatever beta-APP does, it can cause havoc after it has finished its job. Enzymes (shown as scissors in the diagram) slice up the beta-APP. If they do that correctly, the body disposes of the stuff. But if the enzymes miss their target, a critical part of the protein called beta amyloid remains intact. It forms fibrils that then turn up as plaques. Scientists recently determined that -- at least for people with the inherited form of Alzheimer's -- what leads the scissor enzymes astray is a single mutation, a solitary misprint in the genetic code something like a misspelled computer command. That discovery suggests possible points of attack for drugs that could slow the progress of Alzheimer's or even stop it cold. One approach would inhibit those misguided enzymes; another would try to stop the poisoning of neurons by the senile plaques. Leading the way toward such new medications is Athena Neurosciences Inc., a small publicly held company in South San Francisco. Eli Lilly & Co. is collaborating with Athena and financing its research on Alzheimer's to the tune of nearly $20 million through 1996. Athena's research vice president, Lawrence C. Fritz, helped identify beta-APP and analyze its activity in the brain. He expects prototype drugs to be in clinical testing three to four years from now.